Acute Silicosis Responding to Corticosteroid Therapy

Goodman, George; Kaplan, Peter D.; Stachura, Irene; Castranova, Vincent; Pailes, William H.; Lapp, N. L.

doi:10.1378/chest.101.2.366

Cited by 58 publications

(23 citation statements)

References 11 publications

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“…This greater potency of fresh silica dust has been demonstrated after both in vitro and inhalation exposures of rat alveolar macrophages (86,99). Similarly, extremely high levels of chemiluminescence have been reported from a rock driller who was exposed to fresh silica and was diagnosed with acute siicosis (97).…”

Section: Activation Ofoxidant Species Production By Alveolar Macrophagesmentioning

confidence: 81%

“…As with cytotoxic responses, the degree of pulmonary inflammation is related to the ability of the silica particles to generate radicals, i.e., freshly fractured silica exhibits more surface radicals and causes more PMN recruitment than aged silica (18,86). PMN recruitment has also been demonstrated as a hallmark of acute silicosis in humans (97). Exposure of animals to coal dust also results in inflammation characterized as an increase in the number of macrophages and PMNs in the alveolar space (82,104).…”

Section: Stimulation Ofinflammatory Cytokine Releasementioning

confidence: 99%

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Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

309

176

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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

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Section: Activation Ofoxidant Species Production By Alveolar Macrophagesmentioning

confidence: 81%

Section: Stimulation Ofinflammatory Cytokine Releasementioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

309

176

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“…Induction of ROS from AM has also been reported in silicotic patients. Indeed, both basal 02'-and H202 release are elevated in AM from patients with chronic silicosis (11), whereas both basal and zymosanstimulated CL are increased 12-fold in AM from a rock driller with acute silicosis (12). Recent were anesthetized by intraperitoneal injection of sodium methohexital.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Castranova¹,

Huffman²,

Judy³

et al. 1998

Environmental Health Perspectives

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In vivo exposure of rat lungs to crystalline silica either by intratracheal instillation or by inhalation results in an increase in mRNA levels for inducible nitric oxide synthase (iNOS) in bronchoalveolar lavage cells (BALC), elevated nitric oxide ('NO) production by BALC, and an increase in 'NOdependent chemiluminescence (CL) from alveolar macrophages (AM). Induction of iNOS message occurs in both AM and polymorphonuclear leukocytes (PMN) harvested from silicaexposed lungs but is not significantly elevated in lavaged lung tissue. In vitro exposure of AM to silica does not stimulate 'NO production or enhance iNOS message. However, treatment of naive AM with conditioned media from BALC harvested from silica-exposed rats does increase iNOS message and 'NO production by these AM. The potency of this conditioned medium is dependent on interaction between AM and PMN. In the rat model, a relationship exists between the ability of various dusts to cause PMN recruitment or protein leakage into the alveolar space and the induction of iNOS message in BALC, i.e., silica > coal mine dust > carbonyl iron > titanium dioxide. Similarly, a comparison of BALC from a healthy volunteer, a silica-exposed coal miner with a normal chest radiograph, and a silica-exposed coal miner with an abnormal chest radiograph shows a correlation between pathology and both the level of iNOS message in BALC and the magnitude of 'NO-dependent CL from AM. These data suggest that 'NO may play a role in silicosis and that human pulmonary phagocytes exhibit enhanced 'NO production in response to an inflammatory insult.

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“…Management of the disease involves prevention of progression and reducing the risk of complications [8]. Only partial [24] and transient [27] improvement of acute silicosis may be achieved by corticosteroid therapy. Silicosis may highly increase the risk of lung cancer [28,29] and tuberculosis [30], especially in resource�limited coun� tries [31].…”

Section: Discussionmentioning

confidence: 99%

Different course of silicosis in four brothers of one family

Danila¹,

Šileikienė²,

Nargėla³

et al. 2009

International Journal of Occupational Medicine and Environmental Health

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Silicosis remains a common occupational respiratory disease. Even in this era of highly sophisticated hygiene in European countries, new occupational cases of silicosis continue to be reported. Four cases of silicosis which developed after a rela� . Four cases of silicosis which developed after a rela� tively short occupational exposure to respirable silica among the members of one family are described. Four young men worked illegally abroad in mining in one of European countries. All of them were employed together in the same working conditions. One of the brothers died due to the acute form of the disease (lipoproteinosis). Two of the brothers suffered from simple nodular silicosis, and the fourth brother developed very early nodular silicosis and small airway dust disease. A one year follow�up revealed moderate/severe worsening of the disease in all surviving brothers.

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Acute Silicosis Responding to Corticosteroid Therapy

Cited by 58 publications

References 11 publications

Silicosis and coal workers' pneumoconiosis.

Silicosis and coal workers' pneumoconiosis.

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Different course of silicosis in four brothers of one family

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